La disfagia en cuidados intensivos, un problema real: análisis de factores de riesgo / Dysphagia in intensive care, a real problem: analysis of risk factors

Objetivos: Determinar los factores de riesgo presentes en los pacientes con disfagia en relación con una población de pacientes críticos. Método: Serie de casos de una cohorte de pacientes reclutados en la unidad de cuidados intensivos (UCI) hasta el alta hospitalaria. Se reclutaron a aquellos pacientes que dieron su consentimiento y cumplían los criterios de inclusión. El método de exploración clínica Volumen-Viscosidad fue utilizado para la detección de la disfagia. Se realizó un análisis estadístico uni- y bivariante, a través del odds ratio (OR) para detectar los factores de riesgo en la disfagia. Resultados: 103 pacientes fueron reclutados de 401 posibles. La media de edad fue de 59,33±13,23; los hombres representaban el 76,7%. La gravedad media fue: APACHE II (12,74±6,17) y Charlson (2,98±3,31). Un 45,6% de los pacientes desarrollaron disfagia, obteniendo valores significativos de OR (p<0,050) para el desarrollo de disfagia: la mayor edad, los antecedentes neurológicos, COVID19, la alta estancia en UCI y hospitalización y la presencia de traqueotomía. Los pacientes COVID19 representaban el 46,6%, por lo que se realizó un análisis de este subgrupo observando resultados similares, con un riesgo de Charlson (OR:4,65; IC95%: 1,31-16,47; p=0,014) y una estancia hospitalaria (OR: 8,50; IC95%: 2,20-32,83; p<0,001). Al alta de UCI, el 37,9% de la población presentaba todavía disfagia, y mantenía este problema al alta hospitalaria el 12,6%. Conclusiones: Casi la mitad de nuestros pacientes presentaron disfagia. Fueron factores de riesgo la gravedad clínica y la presencia de traqueotomía. Se observó en estos pacientes una mayor estancia tanto en UCI como en hospitalización.(AU)

Aims: To identify risk factors present in patients with dysphagia in a population of critically ill patients. Methods: Case series of a cohort of patients recruited in the intensive care unit (ICU) until hospital discharge. Patients who gave consent and met the inclusion criteria were recruited. The Volume-Viscosity clinical examination method was used for the screening of dysphagia. An uni- and bivariate statistical analysis was performed using odds ratio (OR) to detect risk factors for dysphagia. Outcomes: 103 patients were recruited from 401 possible. The mean age was 59,33±13,23, men represented 76,7%. The severity of the sample was: APACHE II (12,74±6,17) and Charlson (2,98±3,31). 45,6% of patients showed dysphagia, obtaining significant OR values (p<0,050) for the development of dysphagia: older age, neurological antecedents, COVID19, long stay in ICU and hospitalization, and the presence of tracheotomy. COVID19 patients represented 46,6% of the sample, so an analysis of this subgroup was performed, showing similar results, with a Charlson risk (OR:4,65; 95% CI:1,31-16,47; p=0,014) and a hospital stay (OR: 8,50; 95%CI: 2,20-32,83; p<0,001). On discharge from the ICU, 37,9% of the population still had dysphagia; 12,6% maintained this problem at hospital discharge. Conclusions: Almost half of our patients developed dysphagia. Clinical severity and the presence of tracheotomy were risk factors. We observed in patients with dysphagia a longer stay in both ICU and hospitalization.(AU)

Dysphagia in intensive care, a real problem: analysis of risk factors.

AIMS: To identify risk factors present in patients with dysphagia in a population of critically ill patients. METHODS: Case series of a cohort of patients recruited in the intensive care unit (ICU) until hospital discharge. Patients who gave consent and met the inclusion criteria were recruited. The Volume-Viscosity clinical examination method was used for the screening of dysphagia. An uni- and bivariate statistical analysis was performed using odds ratio (OR) to detect risk factors for dysphagia. OUTCOMES: 103 patients were recruited from 401 possible. The mean age was 59,33 ± 13,23, men represented 76,7%. The severity of the sample was: APACHE II (12,74 ± 6,17) and Charlson (2,98 ± 3,31). 45,6% of patients showed dysphagia, obtaining significant OR values (p < 0,050) for the development of dysphagia: older age, neurological antecedents, COVID19, long stay in ICU and hospitalization, and the presence of tracheotomy. COVID19 patients represented 46,6% of the sample, so an analysis of this subgroup was performed, showing similar results, with a Charlson risk (OR:4,65; 95% CI:1,31-16,47; p = 0,014) and a hospital stay (OR: 8,50; 95%CI: 2,20-32,83; p < 0,001) On discharge from the ICU, 37,9% of the population still had dysphagia; 12,6% maintained this problem at hospital discharge. CONCLUSIONS: Almost half of our patients developed dysphagia. Clinical severity and the presence of tracheotomy were risk factors. We observed in patients with dysphagia a longer stay in both ICU and hospitalization.

Edema pulmonar e insuficiencia renal en paciente adicto a cocaína (crack) / Pulmonary edema and renal failure in cocaine (crack) abuser patient

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Retrotransfer of DNA in the rhizosphere.

Retrotransfer of DNA refers to the phenomenon by which a plasmid travels from a host strain to a recipient one and returns to the original host, bringing with it DNA from the recipient. The resultant host strain with DNA from the recipient is called a retrotransconjugant. The retrotransfer phenomenon mediated by the TOL plasmid pWW0 and other plasmids has been documented on plates under optimal laboratory culture conditions, but never under natural conditions. In this work, we show that retrotransfer mediated by the IncP9 TOL pWW0 plasmid occurs in the rhizosphere, a niche in which the continuous supply of nutrients via root exudates allows cells to reach a high density. This suggests that this unusual sexual fertilization may be of great importance in lateral gene transfer. We also show that retrotransfer of DNA seems to require co-integration of the plasmid and the host chromosome and subsequent resolution, because a TOL plasmid with a mutation in the tnpR gene, encoding the resolvase of the Tn4653 of the TOL plasmid, was self-transferred between Pseudomonas strains, but unable to mobilize chromosome.

Combined physical and genetic map of the Pseudomonas putida KT2440 chromosome.

A combined physical and genetic map of the Pseudomonas putida KT2440 genome was constructed from data obtained by pulsed-field gel electrophoresis techniques (PFGE) and Southern hybridization. Circular genome size was estimated at 6.0 Mb by adding the sizes of 19 SwaI, 9 PmeI, 6 PacI, and 6 I-CeuI fragments. A complete physical map was achieved by combining the results of (i) analysis of PFGE of the DNA fragments resulting from digestion of the whole genome with PmeI, SwaI, I-CeuI, and PacI as well as double digestion with combinations of these enzymes and (ii) Southern hybridization analysis of the whole wild-type genome digested with different enzymes and hybridized against a series of probes obtained as cloned genes from different pseudomonads of rRNA group I and Escherichia coli, as P. putida DNA obtained by PCR amplification based on sequences deposited at the GenBank database, and by labeling of macrorestriction fragments of the P. putida genome eluted from agarose gels. As an alternative, 10 random mini-Tn5-Km mutants of P. putida KT2440 were used as a source of DNA, and the band carrying the mini-Tn5 in each mutant was identified after PFGE of a series of complete chromosomal digestions and hybridization with the kanamycin resistance gene of the mini-Tn5 as a probe. We established a circular genome map with an average resolution of 160 kb. Among the 63 genes located on the genetic map were key markers such as oriC, 6 rrn loci (rnnA to -F), recA, ftsZ, rpoS, rpoD, rpoN, and gyrB; auxotrophic markers; and catabolic genes for the metabolism of aromatic compounds. The genetic map of P. putida KT2440 was compared to those of Pseudomonas aeruginosa PAO1 and Pseudomonas fluorescens SBW25. The chromosomal backbone revealed some similarity in gene clustering among the three pseudomonads but differences in physical organization, probably as a result of intraspecific rearrangements.

Free protein S deficiency in hemodialysis patients due to vascular calcifications?

Vascular calcifications are frequent in hemodialysis patients. Its incidence ranges from 25 to 67% depending of different series. Thirty hemodialysis patients were selected from a dialysis population of 150 patients. These 30 patients were divided into two groups: group I included 15 hemodialysis patients with severe secondary hyperparathyroidism and severe, roentgenographically visible diffuse vascular calcifications, and group II included 15 other hemodialysis patients with moderate hyperparathyroidism without radiographic evidence of arterial calcifications. The control group comprised 20 normal volunteers. In all patients, measurements of protein C activity, free protein S and intact parathyroid hormone (PTH) were performed. Statistical analysis showed that free protein S in the patients of group I had a tendency to be lower than in the patients of group II (p < 0.01) and the control group (p < 0.001). We did not find significant differences in free protein S between group II and control group patients nor a significant correlation between intact PTH and free protein S in groups I and II. Protein C activity was found to be in the normal range in both groups. Free protein S deficiency in patients of group I would suggest a synthesis defect by impaired endothelial cells-due to vascular calcifications (?). Free protein S deficiency could increase the risk of thrombotic complications in these patients.

Chromosomal gene capture mediated by the Pseudomonas putida TOL catabolic plasmid.

The Pseudomonas putida TOL plasmid pWW0 is able to mediate chromosomal mobilization in the canonical unidirectional way, i.e., from donor to recipient cells, and bidirectionally, i.e., donor-->recipient-->donor (retrotransfer). Transconjugants are recipient cells that have received DNA from donor cells, whereas retrotransconjugants are donor bacteria that have received DNA from a recipient. The TOL plasmid pWW0 is able to directly mobilize and retromobilize a kanamycin resistance marker integrated into the chromosome of other P. putida strains, a process that appears to involve a single conjugational event. The rate of retrotransfer (as well as of direct transfer) of the chromosomal marker is influenced by the location of the kanamycin marker on the chromosome and ranges from 10(-3) to less than 10(-8) retrotransconjugants per donor (transconjugants per recipient). The mobilized DNA is incorporated into the chromosome of the retrotransconjugants (transconjugants) in a process that seems to occur through recombination of highly homologous flanking regions. No interspecific mobilization of the chromosomal marker in matings involving P. putida and the closely related Pseudomonas fluorescens, which belongs to rRNA group I, was observed.

Treatment of severe secondary hyperparathyroidism with administration of calcium carbonate, intermittent high oral doses of 1,25-dihydroxyvitamin D3 and dialysate with 3 mEq/1 calcium concentration.

In this study, we evaluated the effect of long-term administration of daily calcium carbonate (2-4 g/day) and intermittent high oral doses of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3, 3-4 micrograms, given twice a week] in conjunction with a 3-mEq/1 calcium concentration in the dialysate for the treatment of severe secondary hyperparathyroidism in 6 hemodialysis patients. All patients had reduced serum levels of 1,25-(OH)2D3, which increased significantly (p < 0.005) reaching the maximum level in the 4th month. Serum total and ionized calcium levels significantly increased also, in relation to those before treatment. No patients developed hypercalcemia. Serum phosphorus did not significantly change during the study. Initial serum intact parathyroid hormone (PTH) (1,241 +/- 233 pg/ml, mean +/- SEM) markedly decreased after starting treatment with 1,25-(OH)2D3, being 542 +/- 174 pg/ml in the 5th month and 477 +/- 174 pg/ml in the 8th month. These changes are statistically significant (p < 0.05 and < 0.007, respectively). Alkaline phosphatase behavior was similar to that of intact PTH. A constant direct correlation between intact PTH and alkaline phosphatase and an inverse significant correlation between intact PTH and 1,25-(OH)2D3 was evidenced by us. We conclude that oral 1,25-(OH)2D3 pulse therapy is very effective in suppressing PTH secretion. The administration of calcium carbonate and the use of dialysate with a reduced calcium concentration would allow to prevent hyperphosphatemia and the administration of high oral doses of 1,25-(OH)2D3 without concomitant hypercalcemia.